The muscle energy recovery speed (ViPCr) responded more clearly to IGF-I than another measure (τPCr), meaning ViPCr might be a better way to track how well muscles are making energy.

The drug didn’t make muscles stronger or change how much energy they used during exercise — only how fast they recovered afterward, which points to mitochondria being the target.

The muscle energy improvement wasn’t because people lost weight or got more active — it seemed to be linked directly to IGF-I levels instead.

Even when accounting for factors like age, weight, and insulin levels, higher IGF-I still links to better muscle energy recovery in obese people with low growth hormone.

When IGF-I levels go up in obese people with low growth hormone, their muscles recover energy faster after exercise, and this connection is statistically significant.

Before starting the study, both the drug group and the placebo group had the same muscle energy recovery ability, so any later differences weren’t due to starting out differently.